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Microftalmia colobomatosa
ORPHA:98938CID-10 · Q11.2CID-11 · LA10.0DOENÇA RARA

É uma condição de desenvolvimento do olho em que um ou os dois olhos são menores do que o normal (microftalmia). Essa condição vem acompanhada de um coloboma, que é uma falha ou fenda em alguma parte da estrutura do olho.

Mantido por Agente Raras·Colaborar como especialista →

Introdução

O que você precisa saber de cara

📋

É uma condição de desenvolvimento do olho em que um ou os dois olhos são menores do que o normal (microftalmia). Essa condição vem acompanhada de um coloboma, que é uma falha ou fenda em alguma parte da estrutura do olho.

Publicações científicas
47 artigos
Último publicado: 2026 Feb 20

Escala de raridade

CLASSIFICAÇÃO ORPHANET · BRASIL 2024
1-5 / 10 000
Ultra-rara
<1/50k
Muito rara
1/20k
Rara
1/10k
Pouco freq.
1/5k
Incomum
1/2k
Prevalência
19.0
United Kingdom
Início
Antenatal
+ neonatal
🏥
SUS: Cobertura mínimaScore: 15%
CID-10: Q11.2
🇧🇷Dados SUS / DATASUS
PROCEDIMENTOS SIGTAP (5)
0202010503
Cariótipo — bandas G, Q ou Rgenetic_test
0202010600
Pesquisa de microdeleções/microduplicações por FISHlab_test
0202010694
Sequenciamento completo do exoma (WES)rehabilitation
0202010260
Dosagem de alfa-fetoproteína
0301070040
Atendimento em reabilitação — doenças raras
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Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Partes do corpo afetadas

👁️
Olhos
26 sintomas
😀
Face
3 sintomas
🧠
Neurológico
3 sintomas
🦴
Ossos e articulações
1 sintomas
👂
Ouvidos
1 sintomas

+ 16 sintomas em outras categorias

Características mais comuns

Filtro longo
Coloboma corioretiniano inferior
Hipermetropia alta
Fotofobia
Coloboma retiniano
Cisto orbital
50sintomas
Sem dados (50)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 50 características clínicas mais associadas, ordenadas por frequência.

Filtro longoLong philtrum
Coloboma corioretiniano inferiorInferior chorioretinal coloboma
Hipermetropia altaHigh hypermetropia
FotofobiaPhotophobia
Coloboma retinianoRetinal coloboma

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1desde 2026
Total histórico47PubMed
Últimos 10 anos15publicações
Pico20254 papers
Linha do tempo
2026Hoje · 2026📈 2025Ano de pico
Publicações por ano (últimos 10 anos)

Encontrou um erro ou informação desatualizada? Sugira uma correção →

Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

16 genes identificados com associação a esta condição. Padrão de herança: Autosomal dominant, Autosomal recessive.

SOX2Transcription factor SOX-2Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Transcription factor that forms a trimeric complex with OCT4 on DNA and controls the expression of a number of genes involved in embryonic development such as YES1, FGF4, UTF1 and ZFP206 (By similarity). Binds to the proximal enhancer region of NANOG (By similarity). Critical for early embryogenesis and for embryonic stem cell pluripotency (PubMed:18035408). Downstream SRRT target that mediates the promotion of neural stem cell self-renewal (By similarity). Keeps neural cells undifferentiated by

LOCALIZAÇÃO

Nucleus speckleCytoplasmNucleus

VIAS BIOLÓGICAS (10)
Formation of the posterior neural plateDeactivation of the beta-catenin transactivating complexInterleukin-4 and Interleukin-13 signalingGerm layer formation at gastrulationTranscriptional regulation of pluripotent stem cells
MECANISMO DE DOENÇA

Microphthalmia, syndromic, 3

A disease characterized by the rare association of malformations including uni- or bilateral anophthalmia or microphthalmia, and esophageal atresia with trachoesophageal fistula. Microphthalmia is a disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues (anophthalmia). In many cases, microphthalmia/anophthalmia occurs in association with syndromes that include non-ocular abnormalities.

EXPRESSÃO TECIDUAL(Ubíquo)
Cérebro - Amígdala
69.8 TPM
Brain Caudate basal ganglia
68.0 TPM
Brain Nucleus accumbens basal ganglia
67.1 TPM
Brain Anterior cingulate cortex BA24
66.8 TPM
Brain Frontal Cortex BA9
57.5 TPM
OUTRAS DOENÇAS (4)
anophthalmia/microphthalmia-esophageal atresia syndromemicrophthalmia, isolated, with colobomananophthalmiaseptooptic dysplasia
HGNC:11195UniProt:P48431
NHEJ1Non-homologous end-joining factor 1Disease-causing germline mutation(s) inTolerante
FUNÇÃO

DNA repair protein involved in DNA non-homologous end joining (NHEJ); it is required for double-strand break (DSB) repair and V(D)J recombination and is also involved in telomere maintenance (PubMed:16439204, PubMed:16439205, PubMed:17317666, PubMed:17470781, PubMed:17717001, PubMed:18158905, PubMed:18644470, PubMed:20558749, PubMed:26100018, PubMed:28369633). Plays a key role in NHEJ by promoting the ligation of various mismatched and non-cohesive ends (PubMed:17470781, PubMed:17717001, PubMed:

LOCALIZAÇÃO

NucleusChromosome

VIAS BIOLÓGICAS (1)
Nonhomologous End-Joining (NHEJ)
MECANISMO DE DOENÇA

Immunodeficiency 124, severe combined

A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia and low or absent antibody levels. Patients with SCID present in infancy with recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T- cell development. IMD124 is characterized by a profound T- and B- lymphocytopenia associated with increased cellular sensitivity to ionizing radiation, shortened telomeres and premature senescence of hematopoietic stem cells, microcephaly and growth retardation. Some patients may manifest SCID with sensitivity to ionizing radiation without microcephaly and mild growth retardation, probably due to hypomorphic NHEJ1 variants.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
23.6 TPM
Cervix Ectocervix
18.7 TPM
Útero
16.8 TPM
Cólon transverso
15.3 TPM
Cervix Endocervix
14.9 TPM
OUTRAS DOENÇAS (2)
microphthalmia/coloboma 13Cernunnos-XLF deficiency
HGNC:25737UniProt:Q9H9Q4
FZD5Frizzled-5Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Receptor for Wnt proteins (PubMed:10097073, PubMed:20530549, PubMed:26908622, PubMed:9054360). Functions in the canonical Wnt/beta-catenin signaling pathway. In vitro activates WNT2, WNT10B, WNT5A, but not WNT2B or WNT4 signaling (By similarity). In neurons, activation by WNT7A promotes formation of synapses (PubMed:20530549). May be involved in transduction and intercellular transmission of polarity information during tissue morphogenesis and/or in differentiated tissues (Probable). Plays a rol

LOCALIZAÇÃO

Cell membraneGolgi apparatus membraneSynapsePerikaryonCell projection, dendriteCell projection, axon

VIAS BIOLÓGICAS (7)
Ca2+ pathwayAsymmetric localization of PCP proteinsWNT5A-dependent internalization of FZD2, FZD5 and ROR2Disassembly of the destruction complex and recruitment of AXIN to the membraneRegulation of FZD by ubiquitination
MECANISMO DE DOENÇA

Microphthalmia/Coloboma 11

A form of colobomatous microphthalmia, a disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like coloboma, opacities of the cornea and lens, scaring of the retina and choroid, and other abnormalities may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure). MCOPCB11 is an autosomal dominant form with incomplete penetrance.

EXPRESSÃO TECIDUAL(Ubíquo)
Cólon transverso
27.6 TPM
Cólon sigmoide
18.0 TPM
Fígado
17.0 TPM
Tireoide
15.5 TPM
Estômago
13.4 TPM
OUTRAS DOENÇAS (7)
microphthalmia/coloboma 11coloboma of eyelidcoloboma of choroid and retinacoloboma of macula
HGNC:4043UniProt:Q13467
STRA6Receptor for retinol uptake STRA6Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Functions as a retinol transporter. Accepts all-trans retinol from the extracellular retinol-binding protein RBP4, facilitates retinol transport across the cell membrane, and then transfers retinol to the cytoplasmic retinol-binding protein RBP1 (PubMed:18316031, PubMed:22665496, PubMed:9452451). Retinol uptake is enhanced by LRAT, an enzyme that converts retinol to all-trans retinyl esters, the storage forms of vitamin A (PubMed:18316031, PubMed:22665496). Contributes to the activation of a sig

LOCALIZAÇÃO

Cell membrane

VIAS BIOLÓGICAS (1)
The canonical retinoid cycle in rods (twilight vision)
MECANISMO DE DOENÇA

Microphthalmia, syndromic, 9

A rare clinical entity including as main characteristics anophthalmia or severe microphthalmia, and pulmonary hypoplasia or aplasia. Microphthalmia is a disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues (anophthalmia). In many cases, microphthalmia/anophthalmia occurs in association with syndromes that include non-ocular abnormalities.

EXPRESSÃO TECIDUAL(Tecido-específico)
Cervix Endocervix
19.8 TPM
Pituitária
9.0 TPM
Testículo
7.5 TPM
Cervix Ectocervix
7.1 TPM
Próstata
6.0 TPM
OUTRAS DOENÇAS (2)
Matthew-Wood syndromemicrophthalmia, isolated, with coloboma
HGNC:30650UniProt:Q9BX79
RAXInterferon-inducible double-stranded RNA-dependent protein kinase activator ADisease-causing germline mutation(s) inTolerante
FUNÇÃO

Activates EIF2AK2/PKR in the absence of double-stranded RNA (dsRNA), leading to phosphorylation of EIF2S1/EFI2-alpha and inhibition of translation and induction of apoptosis. Required for siRNA production by DICER1 and for subsequent siRNA-mediated post-transcriptional gene silencing. Does not seem to be required for processing of pre-miRNA to miRNA by DICER1. Promotes UBC9-p53/TP53 association and sumoylation and phosphorylation of p53/TP53 at 'Lys-386' at 'Ser-392' respectively and enhances it

LOCALIZAÇÃO

Cytoplasm, perinuclear regionCytoplasm

VIAS BIOLÓGICAS (2)
MicroRNA (miRNA) biogenesisSmall interfering RNA (siRNA) biogenesis
MECANISMO DE DOENÇA

Dystonia 16

An early-onset dystonia-parkinsonism disorder. Dystonia is defined by the presence of sustained involuntary muscle contraction, often leading to abnormal postures. DYT16 patients have progressive, generalized dystonia with axial muscle involvement, oro-mandibular (sardonic smile) and laryngeal dystonia and, in some cases, parkinsonian features.

EXPRESSÃO TECIDUAL(Não detectado)
Pituitária
0.3 TPM
Testículo
0.2 TPM
Skin Not Sun Exposed Suprapubic
0.2 TPM
Skin Sun Exposed Lower leg
0.2 TPM
Brain Nucleus accumbens basal ganglia
0.1 TPM
OUTRAS DOENÇAS (3)
isolated microphthalmia 3nanophthalmiamicrophthalmia, isolated, with coloboma
HGNC:18662UniProt:O75569
SIX6Homeobox protein SIX6Candidate gene tested inTolerante
FUNÇÃO

May be involved in eye development

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Optic disk anomalies with retinal and/or macular dystrophy

An ocular disorder characterized by optic nerve dysplasia, optic disk anomalies, chorioretinal dystrophy and macular atrophy. Some patients have microphthalmia.

EXPRESSÃO TECIDUAL(Tecido-específico)
Pituitária
55.2 TPM
Hipotálamo
1.1 TPM
Testículo
0.4 TPM
Músculo esquelético
0.2 TPM
Próstata
0.1 TPM
OUTRAS DOENÇAS (3)
colobomatous optic disc-macular atrophy-chorioretinopathy syndromenanophthalmiamicrophthalmia, isolated, with coloboma
HGNC:10892UniProt:O95475
GDF3Growth/differentiation factor 3Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Growth factor involved in early embryonic development and adipose-tissue homeostasis. During embryogenesis controls formation of anterior visceral endoderm and mesoderm and the establishment of anterior-posterior identity through a receptor complex comprising the receptor ACVR1B and the coreceptor CRIPTO (By similarity). Regulates adipose-tissue homeostasis and energy balance under nutrient overload in part by signaling through the receptor complex based on ACVR1C and CRIPTO/Cripto (PubMed:21805

LOCALIZAÇÃO

SecretedCytoplasm

MECANISMO DE DOENÇA

Klippel-Feil syndrome 3, autosomal dominant

A skeletal disorder characterized by congenital fusion of cervical vertebrae. It is due to a failure in the normal segmentation of vertebrae during the early weeks of fetal development. The clinical triad consists of short neck, low posterior hairline, and limited neck movement.

EXPRESSÃO TECIDUAL(Baixa expressão)
Rim - Medula
2.6 TPM
Baço
1.3 TPM
Testículo
0.4 TPM
Glândula adrenal
0.3 TPM
Tecido adiposo
0.3 TPM
OUTRAS DOENÇAS (5)
Klippel-Feil syndrome 3, autosomal dominantisolated microphthalmia 7microphthalmia, isolated, with coloboma 6microphthalmia, isolated, with coloboma
HGNC:4218UniProt:Q9NR23
TENM3Teneurin-3Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Involved in neural development by regulating the establishment of proper connectivity within the nervous system. Acts in both pre- and postsynaptic neurons in the hippocampus to control the assembly of a precise topographic projection: required in both CA1 and subicular neurons for the precise targeting of proximal CA1 axons to distal subiculum, probably by promoting homophilic cell adhesion. Required for proper dendrite morphogenesis and axon targeting in the vertebrate visual system, thereby p

LOCALIZAÇÃO

Cell membraneCell projection, axon

MECANISMO DE DOENÇA

Microphthalmia/Coloboma 9

A disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, and other abnormalities may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).

EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
14.6 TPM
Nervo tibial
10.7 TPM
Pituitária
8.3 TPM
Cólon sigmoide
7.8 TPM
Glândula adrenal
6.0 TPM
INTERAÇÕES PROTEICAS (3)
OUTRAS DOENÇAS (2)
microphthalmia, isolated, with coloboma 9microphthalmia, isolated, with coloboma
HGNC:29944UniProt:Q9P273
ABCB6ATP-binding cassette sub-family B member 6Disease-causing germline mutation(s) inTolerante
FUNÇÃO

ATP-dependent transporter that catalyzes the transport of a broad-spectrum of porphyrins from the cytoplasm to the extracellular space through the plasma membrane or into the vesicle lumen (PubMed:17661442, PubMed:23792964, PubMed:27507172, PubMed:33007128). May also function as an ATP-dependent importer of porphyrins from the cytoplasm into the mitochondria, in turn may participate in the de novo heme biosynthesis regulation and in the coordination of heme and iron homeostasis during phenylhydr

LOCALIZAÇÃO

Cell membraneMitochondrion outer membraneEndoplasmic reticulum membraneGolgi apparatus membraneEndosome membraneLysosome membraneLate endosome membraneEarly endosome membraneSecreted, extracellular exosomeMitochondrionEndosome, multivesicular body membraneMelanosome membrane

VIAS BIOLÓGICAS (1)
Mitochondrial ABC transporters
MECANISMO DE DOENÇA

Microphthalmia/Coloboma 7

A disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, and other abnormalities may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).

OUTRAS DOENÇAS (12)
microphthalmia, isolated, with coloboma 7familial pseudohyperkalemiadyschromatosis universalis hereditaria 3obsolete blood group, langereis system
HGNC:47UniProt:Q9NP58
SHHSonic hedgehog proteinDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

The C-terminal part of the sonic hedgehog protein precursor displays an autoproteolysis and a cholesterol transferase activity (By similarity). Both activities result in the cleavage of the full-length protein into two parts (ShhN and ShhC) followed by the covalent attachment of a cholesterol moiety to the C-terminal of the newly generated ShhN (By similarity). Both activities occur in the endoplasmic reticulum (By similarity). Once cleaved, ShhC is degraded in the endoplasmic reticulum (By simi

LOCALIZAÇÃO

Endoplasmic reticulum membraneGolgi apparatus membraneSecretedCell membrane

VIAS BIOLÓGICAS (5)
Hedgehog 'on' stateActivation of SMOLigand-receptor interactionsRelease of Hh-Np from the secreting cellFormation of lateral plate mesoderm
MECANISMO DE DOENÇA

Microphthalmia/Coloboma 5

A disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, and other abnormalities may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).

EXPRESSÃO TECIDUAL(Tecido-específico)
Nervo tibial
21.7 TPM
Glândula adrenal
7.7 TPM
Fígado
7.4 TPM
Estômago
3.8 TPM
Rim - Medula
3.5 TPM
OUTRAS DOENÇAS (15)
microphthalmia, isolated, with coloboma 5holoprosencephaly 3solitary median maxillary central incisor syndrometibia, hypoplasia or aplasia of, with polydactyly
HGNC:10848UniProt:Q15465
PORCNProtein-serine O-palmitoleoyltransferase porcupineDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Protein-serine O-palmitoleoyltransferase that acts as a key regulator of the Wnt signaling pathway by mediating the attachment of palmitoleate, a 16-carbon monounsaturated fatty acid (C16:1(9Z)), to Wnt proteins. Serine palmitoleoylation of WNT proteins is required for efficient binding to frizzled receptors

LOCALIZAÇÃO

Endoplasmic reticulum membrane

VIAS BIOLÓGICAS (2)
WNT ligand biogenesis and traffickingLGK974 inhibits PORCN
MECANISMO DE DOENÇA

Focal dermal hypoplasia

A rare congenital ectomesodermal disorder characterized by a combination of skin defects, skeletal abnormalities, and ocular anomalies. Affected individuals have patchy dermal hypoplasia, often in a distribution pattern following the Blaschko lines, and areas of subcutaneous fat herniation or deposition of fat into the dermis. In addition, sparse and brittle hair, hypoplastic nails and papillomas have been described. Skeletal abnormalities usually comprise syndactyly, ectrodactyly, and brachydactyly, and in some cases osteopathia striata has been seen. Patients frequently have ocular anomalies, including microphthalmia/ anophthalmia, coloboma, pigmentary and vascularization defects of the retina. Dental abnormalities are often present.

EXPRESSÃO TECIDUAL(Ubíquo)
Glândula adrenal
61.6 TPM
Cerebelo
49.8 TPM
Cérebro - Hemisfério cerebelar
46.1 TPM
Fibroblastos
23.7 TPM
Cervix Endocervix
21.3 TPM
OUTRAS DOENÇAS (2)
focal dermal hypoplasiamicrophthalmia, isolated, with coloboma
HGNC:17652UniProt:Q9H237
RBP4Retinol-binding protein 4Disease-causing germline mutation(s) inRestrito
FUNÇÃO

Retinol-binding protein that mediates retinol transport in blood plasma (PubMed:5541771). Delivers retinol from the liver stores to the peripheral tissues (Probable). Transfers the bound all-trans retinol to STRA6, that then facilitates retinol transport across the cell membrane (PubMed:22665496)

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (1)
Retinoid metabolism disease events
MECANISMO DE DOENÇA

Retinal dystrophy, iris coloboma, and comedogenic acne syndrome

A disease characterized by retinal degeneration, ocular colobomas involving both the anterior and posterior segment, impaired night vision and loss of visual acuity. Additional characteristic features include developmental abnormalities and severe acne.

EXPRESSÃO TECIDUAL(Ubíquo)
Fígado
4153.5 TPM
Tecido adiposo
554.2 TPM
Pituitária
376.5 TPM
Adipose Visceral Omentum
289.3 TPM
Mama
162.8 TPM
OUTRAS DOENÇAS (3)
progressive retinal dystrophy due to retinol transport defectmicrophthalmia, isolated, with coloboma 10microphthalmia, isolated, with coloboma
HGNC:9922UniProt:P02753
ALDH1A3Retinaldehyde dehydrogenase 3Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Catalyzes the NAD-dependent oxidation of aldehyde substrates, such as all-trans-retinal and all-trans-13,14-dihydroretinal, to their corresponding carboxylic acids, all-trans-retinoate and all-trans-13,14-dihydroretinoate, respectively (By similarity) (PubMed:27759097). High specificity for all-trans-retinal as substrate, can also accept acetaldehyde as substrate in vitro but with lower affinity (PubMed:27759097). Required for the biosynthesis of normal levels of retinoate in the embryonic ocula

LOCALIZAÇÃO

Cytoplasm

VIAS BIOLÓGICAS (5)
RA biosynthesis pathwayDevelopmental Lineage of Mammary Gland Luminal Epithelial CellsDevelopmental Lineage of Mammary Gland Alveolar CellsDevelopmental Lineage of Mammary Stem CellsDevelopmental Lineage of Mammary Gland Myoepithelial Cells
MECANISMO DE DOENÇA

Microphthalmia, isolated, 8

A disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, and other abnormalities may also be present.

OUTRAS DOENÇAS (3)
isolated microphthalmia 8nanophthalmiamicrophthalmia, isolated, with coloboma
HGNC:409UniProt:P47895
VSX2Visual system homeobox 2Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Acts as a transcriptional regulator through binding to DNA at the consensus sequence 5'-[TC]TAATT[AG][AG]-3' upstream of gene promoters (PubMed:27301076). Plays a significant role in the specification and morphogenesis of the sensory retina (By similarity). May play a role in specification of V2a interneurons during spinal cord development (By similarity). Mediates differentiation of V2a interneurons by repression of motor neuron gene transcription, via competitively binding to response elements

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Microphthalmia, isolated, 2

A disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, and other abnormalities may also be present.

EXPRESSÃO TECIDUAL(Baixa expressão)
Testículo
0.7 TPM
Brain Spinal cord cervical c-1
0.2 TPM
Brain Nucleus accumbens basal ganglia
0.2 TPM
Brain Caudate basal ganglia
0.1 TPM
Cérebro - Hemisfério cerebelar
0.1 TPM
OUTRAS DOENÇAS (3)
isolated microphthalmia 2microphthalmia, isolated, with coloboma 3microphthalmia, isolated, with coloboma
HGNC:1975UniProt:P58304
GDF6Growth/differentiation factor 6Candidate gene tested inAltamente restrito
FUNÇÃO

Growth factor that controls proliferation and cellular differentiation in the retina and bone formation. Plays a key role in regulating apoptosis during retinal development. Establishes dorsal-ventral positional information in the retina and controls the formation of the retinotectal map (PubMed:23307924). Required for normal formation of bones and joints in the limbs, skull, digits and axial skeleton. Plays a key role in establishing boundaries between skeletal elements during development. Regu

LOCALIZAÇÃO

Secreted

MECANISMO DE DOENÇA

Klippel-Feil syndrome 1, autosomal dominant

A skeletal disorder characterized by congenital fusion of cervical vertebrae. It is due to a failure in the normal segmentation of vertebrae during the early weeks of fetal development. The clinical triad consists of short neck, low posterior hairline, and limited neck movement. Deafness is a feature in some cases and may be of sensorineural, conductive, or mixed type.

EXPRESSÃO TECIDUAL(Baixa expressão)
Fibroblastos
2.7 TPM
Útero
2.6 TPM
Coração - Átrio
2.5 TPM
Adipose Visceral Omentum
2.2 TPM
Artéria coronária
2.2 TPM
OUTRAS DOENÇAS (9)
isolated microphthalmia 4multiple synostoses syndrome 4Klippel-Feil syndrome 1, autosomal dominantmicrophthalmia, isolated, with coloboma 6
HGNC:4221UniProt:Q6KF10
OTX2Homeobox protein OTX2Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Transcription factor probably involved in the development of the brain and the sense organs. Can bind to the bicoid/BCD target sequence (BTS): 5'-TCTAATCCC-3'

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (2)
Formation of the posterior neural plateFormation of the anterior neural plate
MECANISMO DE DOENÇA

Microphthalmia, syndromic, 5

Patients manifest unilateral or bilateral microphthalmia/clinical anophthalmia and variable additional features including pituitary dysfunction, coloboma, microcornea, cataract, retinal dystrophy, hypoplasia or agenesis of the optic nerve, agenesis of the corpus callosum, developmental delay, joint laxity, hypotonia, and seizures. Microphthalmia is a disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues (anophthalmia). In many cases, microphthalmia/anophthalmia occurs in association with syndromes that include non-ocular abnormalities.

EXPRESSÃO TECIDUAL(Tecido-específico)
Cérebro - Hemisfério cerebelar
24.4 TPM
Cerebelo
23.8 TPM
Substância negra
2.9 TPM
Hipotálamo
1.0 TPM
Testículo
0.7 TPM
OUTRAS DOENÇAS (8)
pituitary hormone deficiency, combined, 6syndromic microphthalmia type 5septooptic dysplasiacombined pituitary hormone deficiencies, genetic form
HGNC:8522UniProt:P32243

Variantes genéticas (ClinVar)

315 variantes patogênicas registradas no ClinVar.

🧬 SOX2: NM_003106.4(SOX2):c.215G>A (p.Ser72Asn) ()
🧬 SOX2: NM_003106.4(SOX2):c.90_96del (p.Gly31fs) ()
🧬 SOX2: GRCh37/hg19 3q22.1-29(chr3:132561657-197851986)x3 ()
🧬 SOX2: NM_003106.4(SOX2):c.335C>T (p.Pro112Leu) ()
🧬 SOX2: NM_003106.4(SOX2):c.583C>T (p.Gln195Ter) ()
Ver todas no ClinVar

Classificação de variantes (ClinVar)

Distribuição de 18 variantes classificadas pelo ClinVar.

9
9
Patogênica (50.0%)
VUS (50.0%)
VARIANTES MAIS SIGNIFICATIVAS
LRBA: NM_006439.5(MAB21L2):c.840C>G (p.Tyr280Ter) [Pathogenic]
LRBA: NM_006439.5(MAB21L2):c.498T>G (p.Tyr166Ter) [Conflicting classifications of pathogenicity]
MAB21L2: NM_006439.5(MAB21L2):c.881C>A (p.Ser294Ter) [Pathogenic]
LRBA: NM_006439.5(MAB21L2):c.1A>C (p.Met1Leu) [Likely pathogenic]
MAB21L2: NM_006439.5(MAB21L2):c.151C>G (p.Arg51Gly) [Pathogenic]

Vias biológicas (Reactome)

46 vias biológicas associadas aos genes desta condição.

POU5F1 (OCT4), SOX2, NANOG repress genes related to differentiation POU5F1 (OCT4), SOX2, NANOG activate genes related to proliferation Deactivation of the beta-catenin transactivating complex Transcriptional regulation of pluripotent stem cells Interleukin-4 and Interleukin-13 signaling Transcriptional Regulation by MECP2 Germ layer formation at gastrulation Formation of the anterior neural plate Formation of the posterior neural plate Specification of the neural plate border Transcriptional and post-translational regulation of MITF-M expression and activity Regulation of MITF-M-dependent genes involved in extracellular matrix, focal adhesion and epithelial-to-mesenchymal transition Nonhomologous End-Joining (NHEJ) Class B/2 (Secretin family receptors) Ca2+ pathway Asymmetric localization of PCP proteins Disassembly of the destruction complex and recruitment of AXIN to the membrane Regulation of FZD by ubiquitination WNT5A-dependent internalization of FZD2, FZD5 and ROR2 Signaling by RNF43 mutants The canonical retinoid cycle in rods (twilight vision) Defective visual phototransduction due to STRA6 loss of function MicroRNA (miRNA) biogenesis Small interfering RNA (siRNA) biogenesis PKR-mediated signaling Mitochondrial ABC transporters Defective ABCB6 causes MCOPCB7 Hedgehog ligand biogenesis Hh mutants are degraded by ERAD Release of Hh-Np from the secreting cell Ligand-receptor interactions Hedgehog 'on' state Activation of SMO HHAT G278V doesn't palmitoylate Hh-Np Formation of lateral plate mesoderm Formation of axial mesoderm Developmental Lineage of Multipotent Pancreatic Progenitor Cells WNT ligand biogenesis and trafficking LGK974 inhibits PORCN Retinoid metabolism disease events Retinoid metabolism and transport RA biosynthesis pathway Developmental Lineage of Mammary Gland Luminal Epithelial Cells Developmental Lineage of Mammary Gland Alveolar Cells Developmental Lineage of Mammary Gland Myoepithelial Cells Developmental Lineage of Mammary Stem Cells

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Publicações mais relevantes

Timeline de publicações
15 papers (10 anos)
#1

Intragenic loss-of-function variants in transcription factors MAZ, FOXP1 and SIN3B in colobomatous microphthalmia.

Journal of medical genetics2026 Feb 20

Despite the identification of many genes involved in developmental eye phenotypes, a large percentage of families lack genetic diagnoses, suggesting novel mechanisms remain to be discovered. Large deletions of 16p11.2, 3p14 or 19p13.11 regions involving transcription factors MAZ, FOXP1 and SIN3B, correspondingly, along with other genes, have been previously reported in individuals with neurodevelopmental and variable other features, including ocular coloboma and/or microphthalmia; recently, intragenic variants in FOXP1 and SIN3B have also been shown to cause neurodevelopmental phenotypes, with developmental eye defects reported in a small number of individuals with FOXP1 variants. Through exome sequencing analysis we identified novel splicing variants in MAZ and SIN3B, and a recurrent nonsense allele in FOXP1 in unrelated families affected with colobomatous microphthalmia, all with predicted loss-of-function effects; additionally, we report two new families with coloboma and 16p11.2 genomic deletions including MAZ, one de novo and another inherited from an affected parent. These findings provide further support for a role for FOXP1 in structural eye phenotypes, expanding its spectrum to include colobomatous microphthalmia, and suggest a role for MAZ and SIN3B in human eye development and disease.

#2

Variants in NR6A1 cause a novel oculo vertebral renal syndrome.

Nature communications2025 Jul 03

Colobomatous microphthalmia is a potentially blinding congenital ocular malformation that can present either in isolation or together with other syndromic features. Despite a strong genetic component to disease, many cases lack a molecular diagnosis. We describe an autosomal dominant oculo-vertebral-renal (OVR) syndrome in six independent families characterized by colobomatous microphthalmia, missing vertebrae and congenital kidney abnormalities. Genome sequencing identified six rare variants in the orphan nuclear receptor gene NR6A1 in these families. We performed in silico, cellular, and zebrafish experiments to demonstrate the NR6A1 variants were pathogenic or likely pathogenic for OVR syndrome. Knockdown of either or both zebrafish paralogs of NR6A1 results in abnormal eye, kidney, and somite development, which was rescued by wild-type but not variant NR6A1 mRNA. Illustrating the power of genomic ascertainment in medicine, our study establishes NR6A1 as a critical factor in eye, kidney, and vertebral development, and a pleiotropic gene responsible for OVR syndrome.

#3

Cataract Surgery in Congenital Colobomatous Microphthalmia Associated With Intraorbital Cyst in an Adult.

Case reports in ophthalmological medicine2025

We report a challenging congenital cataract surgery in an adult case of colobomatous microphthalmia associated with intraorbital cyst.

#4

The Arg99Gln Substitution in HNRNPC Is Associated with a Distinctive Clinical Phenotype Characterized by Facial Dysmorphism and Ocular and Cochlear Anomalies.

Genes2025 Feb 01

Background/Objectives: Heterozygous variants in the heterogeneous nuclear ribonucleoprotein C gene (HNRNPC) have recently been reported to cause intellectual developmental disorder-74 (MRD74), a neurodevelopmental disorder with no recurrent diagnostic handles. Affected individuals show variable, non-specific, and subtle dysmorphic features. The degree of developmental delay (DD)/intellectual disability (ID) is also wide, ranging from mild to severe. The mutational spectrum is relatively broad with exon deletions and splice site and frameshift variants distributed along the entire length of the gene leading to HNRNPC loss of function. Only two missense changes located within the RNA-binding motif (RBM) and adjacent linker region of the more abundant isoform (Arg64Trp and Arg99Gln) have been described. Notably, the Arg99Gln amino acid substitution was reported in a subject presenting with a more complex and unique clinical phenotype characterized by distinctive facial features, DD/ID, cochlear aplasia, and bilateral colobomatous microphthalmia, suggesting the possible occurrence of phenotypic heterogeneity. Results: Here, we report the second individual carrying the Arg99Gln change in HNRNPC and having clinical features with a significant overlap with the peculiar phenotype of the previously described subject, supporting the occurrence of a genotype-phenotype correlation. Conclusions: Due to the concomitant occurrence of ocular and cochlear involvement as recognizable diagnostic handles, we propose that the HNRNPCArg99Gln-related phenotype should be considered as a potential differential diagnosis in subjects with ID and major signs of CHARGE syndrome not fulfilling the minimum criteria for a clinical diagnosis.

#5

[Bilateral colobomatous microphthalmia with unilateral orbital cyst].

Journal francais d'ophtalmologie2025 Jan

Publicações recentes

Ver todas no PubMed

📚 EuropePMC22 artigos no totalmostrando 14

2026

Intragenic loss-of-function variants in transcription factors MAZ, FOXP1 and SIN3B in colobomatous microphthalmia.

Journal of medical genetics
2025

Cataract Surgery in Congenital Colobomatous Microphthalmia Associated With Intraorbital Cyst in an Adult.

Case reports in ophthalmological medicine
2025

Variants in NR6A1 cause a novel oculo vertebral renal syndrome.

Nature communications
2025

The Arg99Gln Substitution in HNRNPC Is Associated with a Distinctive Clinical Phenotype Characterized by Facial Dysmorphism and Ocular and Cochlear Anomalies.

Genes
2024

Variants in NR6A1 cause a novel oculo-vertebral-renal (OVR) syndrome.

Research square
2025

[Bilateral colobomatous microphthalmia with unilateral orbital cyst].

Journal francais d'ophtalmologie
2022

De novo frameshift mutation in YAP1 associated with bilateral uveal coloboma and microphthalmia.

Ophthalmic genetics
2022

Novel mutation in TENM3 gene in an Iranian patient with colobomatous microphthalmia.

Clinical case reports
2020

Compound heterozygous splicing CDON variants result in isolated ocular coloboma.

Clinical genetics
2019

Homozygous frameshift mutations in FAT1 cause a syndrome characterized by colobomatous-microphthalmia, ptosis, nephropathy and syndactyly.

Nature communications
2019

Sequence variations in TENM3 gene causing eye anomalies with intellectual disability: Expanding the phenotypic spectrum.

European journal of medical genetics
2015

A Case of Anterior Segment Dysgenesis with Iridolenticular Adhesions in Trisomy 18.

Journal of pediatric genetics
2016

Confirmation of TENM3 involvement in autosomal recessive colobomatous microphthalmia.

American journal of medical genetics. Part A
2016

Bosma arhinia microphthalmia syndrome: Clinical report and review of the literature.

American journal of medical genetics. Part A
Ver todos os 22 no EuropePMC

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Referências e fontes

Bases de dados externas citadas neste artigo

Publicações científicas

Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.

  1. Intragenic loss-of-function variants in transcription factors MAZ, FOXP1 and SIN3B in colobomatous microphthalmia.
    Journal of medical genetics· 2026· PMID 41339071mais citado
  2. Variants in NR6A1 cause a novel oculo vertebral renal syndrome.
    Nature communications· 2025· PMID 40610405mais citado
  3. Cataract Surgery in Congenital Colobomatous Microphthalmia Associated With Intraorbital Cyst in an Adult.
    Case reports in ophthalmological medicine· 2025· PMID 41256338mais citado
  4. The Arg99Gln Substitution in HNRNPC Is Associated with a Distinctive Clinical Phenotype Characterized by Facial Dysmorphism and Ocular and Cochlear Anomalies.
    Genes· 2025· PMID 40004505mais citado
  5. [Bilateral colobomatous microphthalmia with unilateral orbital cyst].
    Journal francais d'ophtalmologie· 2025· PMID 39424520mais citado
  6. Variants in NR6A1 cause a novel oculo-vertebral-renal (OVR) syndrome.
    Res Sq· 2024· PMID 39606449recente

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:98938(Orphanet)
  2. MONDO:0000170(MONDO)
  3. GARD:3644(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Q55999509(Wikidata)

Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.

Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar

Microftalmia colobomatosa
Compêndio · Raras BR

Microftalmia colobomatosa

ORPHA:98938 · MONDO:0000170
Prevalência
1-5 / 10 000
Herança
Autosomal dominant, Autosomal recessive
CID-10
Q11.2 · Microftalmia
CID-11
Início
Antenatal, Neonatal
Prevalência
19.0 (United Kingdom)
MedGen
UMLS
C2931501
EuropePMC
Wikidata
Papers 10a
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